Involvement of p38 MAP kinase and Smad3 in TGF-β-mediated mast cell functions

Masayuki Funaba; Teruo Ikeda; Masaru Murakami; Kenji Ogawa; Yoshii Nishino; Kunihiro Tsuchida; Hiromu Sugino; Matanobu Abe

doi:10.1016/j.cellsig.2006.04.005

Involvement of p38 MAP kinase and Smad3 in TGF-β-mediated mast cell functions

Masayuki Funaba, Teruo Ikeda, Masaru Murakami, Kenji Ogawa, Yoshii Nishino, Kunihiro Tsuchida, Hiromu Sugino, Matanobu Abe

Research output: Contribution to journal › Article › peer-review

11 Citations (Scopus)

Abstract

Transforming growth factor-β (TGF-β) modulates functions of bone marrow-derived cultured mast cells (BMMCs); cell maturation (up-regulation of mouse mast cell proteases (mmcps)), growth arrest and migration. We investigated the roles of p38 MAP kinase and Smad3 in TGF-β-mediated cell responses in BMMCs. Treating BMMCs with TGF-β induced the phosphorylation of p38 within 2 h and persisted for 24 h. The involvement of p38 in TGF-β-induced cell responses depended upon mast cell functions; it was necessary for up-regulation of mmcp-1 and migration, but not for up-regulation of mmcp-7 and inhibition of metabolic activity. New protein synthesis was required for the up-regulation of mmcp-1 but not mmcp-7 in response to TGF-β treatment, and stabilization of mRNA was partially responsible for the increase in gene transcript of mmcp-1. The decrease in metabolic activity in response to TGF-β treatment was smaller in Smad3-deficient BMMCs compared to wild-type BMMCs. Maximal migration was detected at a TGF-β concentration of 40 fM in wild-type BMMCs, whereas TGF-β-induced migration was absent in Smad3-deficient BMMCs. Thus, the roles of p38 and Smad3 are different among TGF-β-mediated cell responses in BMMCs.

Original language	English
Pages (from-to)	2154-2161
Number of pages	8
Journal	Cellular Signalling
Volume	18
Issue number	12
DOIs	https://doi.org/10.1016/j.cellsig.2006.04.005
Publication status	Published - 12-2006
Externally published	Yes

All Science Journal Classification (ASJC) codes

Cell Biology

Access to Document

10.1016/j.cellsig.2006.04.005

Cite this

@article{0737bb6e3329406fb1063546186be51f,

title = "Involvement of p38 MAP kinase and Smad3 in TGF-β-mediated mast cell functions",

abstract = "Transforming growth factor-β (TGF-β) modulates functions of bone marrow-derived cultured mast cells (BMMCs); cell maturation (up-regulation of mouse mast cell proteases (mmcps)), growth arrest and migration. We investigated the roles of p38 MAP kinase and Smad3 in TGF-β-mediated cell responses in BMMCs. Treating BMMCs with TGF-β induced the phosphorylation of p38 within 2 h and persisted for 24 h. The involvement of p38 in TGF-β-induced cell responses depended upon mast cell functions; it was necessary for up-regulation of mmcp-1 and migration, but not for up-regulation of mmcp-7 and inhibition of metabolic activity. New protein synthesis was required for the up-regulation of mmcp-1 but not mmcp-7 in response to TGF-β treatment, and stabilization of mRNA was partially responsible for the increase in gene transcript of mmcp-1. The decrease in metabolic activity in response to TGF-β treatment was smaller in Smad3-deficient BMMCs compared to wild-type BMMCs. Maximal migration was detected at a TGF-β concentration of 40 fM in wild-type BMMCs, whereas TGF-β-induced migration was absent in Smad3-deficient BMMCs. Thus, the roles of p38 and Smad3 are different among TGF-β-mediated cell responses in BMMCs.",

author = "Masayuki Funaba and Teruo Ikeda and Masaru Murakami and Kenji Ogawa and Yoshii Nishino and Kunihiro Tsuchida and Hiromu Sugino and Matanobu Abe",

note = "Funding Information: We thank Drs. Takuya Murata, Akira Abe and Miki Hiraoka for critical reviewing of this manuscript. This work was supported by a Grant-in-Aid for Scientific Research (13760214 and 15580268 to M.F. and 16580248 to T.I.) from Japan Society for the Promotion of Science and grants for Graduate Schools from The Foundation for Japanese Private School Promotion (to M.F., T.I. and M.M.).",

year = "2006",

month = dec,

doi = "10.1016/j.cellsig.2006.04.005",

language = "English",

volume = "18",

pages = "2154--2161",

journal = "Cellular Signalling",

issn = "0898-6568",

publisher = "Elsevier Inc.",

number = "12",

}

TY - JOUR

T1 - Involvement of p38 MAP kinase and Smad3 in TGF-β-mediated mast cell functions

AU - Funaba, Masayuki

AU - Ikeda, Teruo

AU - Murakami, Masaru

AU - Ogawa, Kenji

AU - Nishino, Yoshii

AU - Tsuchida, Kunihiro

AU - Sugino, Hiromu

AU - Abe, Matanobu

N1 - Funding Information: We thank Drs. Takuya Murata, Akira Abe and Miki Hiraoka for critical reviewing of this manuscript. This work was supported by a Grant-in-Aid for Scientific Research (13760214 and 15580268 to M.F. and 16580248 to T.I.) from Japan Society for the Promotion of Science and grants for Graduate Schools from The Foundation for Japanese Private School Promotion (to M.F., T.I. and M.M.).

PY - 2006/12

Y1 - 2006/12

N2 - Transforming growth factor-β (TGF-β) modulates functions of bone marrow-derived cultured mast cells (BMMCs); cell maturation (up-regulation of mouse mast cell proteases (mmcps)), growth arrest and migration. We investigated the roles of p38 MAP kinase and Smad3 in TGF-β-mediated cell responses in BMMCs. Treating BMMCs with TGF-β induced the phosphorylation of p38 within 2 h and persisted for 24 h. The involvement of p38 in TGF-β-induced cell responses depended upon mast cell functions; it was necessary for up-regulation of mmcp-1 and migration, but not for up-regulation of mmcp-7 and inhibition of metabolic activity. New protein synthesis was required for the up-regulation of mmcp-1 but not mmcp-7 in response to TGF-β treatment, and stabilization of mRNA was partially responsible for the increase in gene transcript of mmcp-1. The decrease in metabolic activity in response to TGF-β treatment was smaller in Smad3-deficient BMMCs compared to wild-type BMMCs. Maximal migration was detected at a TGF-β concentration of 40 fM in wild-type BMMCs, whereas TGF-β-induced migration was absent in Smad3-deficient BMMCs. Thus, the roles of p38 and Smad3 are different among TGF-β-mediated cell responses in BMMCs.

AB - Transforming growth factor-β (TGF-β) modulates functions of bone marrow-derived cultured mast cells (BMMCs); cell maturation (up-regulation of mouse mast cell proteases (mmcps)), growth arrest and migration. We investigated the roles of p38 MAP kinase and Smad3 in TGF-β-mediated cell responses in BMMCs. Treating BMMCs with TGF-β induced the phosphorylation of p38 within 2 h and persisted for 24 h. The involvement of p38 in TGF-β-induced cell responses depended upon mast cell functions; it was necessary for up-regulation of mmcp-1 and migration, but not for up-regulation of mmcp-7 and inhibition of metabolic activity. New protein synthesis was required for the up-regulation of mmcp-1 but not mmcp-7 in response to TGF-β treatment, and stabilization of mRNA was partially responsible for the increase in gene transcript of mmcp-1. The decrease in metabolic activity in response to TGF-β treatment was smaller in Smad3-deficient BMMCs compared to wild-type BMMCs. Maximal migration was detected at a TGF-β concentration of 40 fM in wild-type BMMCs, whereas TGF-β-induced migration was absent in Smad3-deficient BMMCs. Thus, the roles of p38 and Smad3 are different among TGF-β-mediated cell responses in BMMCs.

UR - http://www.scopus.com/inward/record.url?scp=33750356211&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33750356211&partnerID=8YFLogxK

U2 - 10.1016/j.cellsig.2006.04.005

DO - 10.1016/j.cellsig.2006.04.005

M3 - Article

C2 - 16750902

AN - SCOPUS:33750356211

SN - 0898-6568

VL - 18

SP - 2154

EP - 2161

JO - Cellular Signalling

JF - Cellular Signalling

IS - 12

ER -

Involvement of p38 MAP kinase and Smad3 in TGF-β-mediated mast cell functions

Abstract

All Science Journal Classification (ASJC) codes

Access to Document

Other files and links

Fingerprint

Cite this